Onset Of Autoimmune Thyroid Diseases Research Articles

Vitamin D: An Essential Nutrient in the Dual Relationship between Autoimmune Thyroid Diseases and Celiac Disease-A Comprehensive Review.

Autoimmune thyroid diseases (AITD) are among the most frequent autoimmune disorders, with a multifactorial etiology in which both genetic and environmental determinants are probably involved. Celiac disease (CeD) also represents a public concern, given its increasing prevalence due to the recent improvement of screening programs, leading to the detection of silent subtypes. The two conditions may be closely associated due to common risk factors, including genetic setting, changes in the composition and diversity of the gut microbiota, and deficiency of nutrients like vitamin D. This comprehensive review discussed the current evidence on the pivotal role of vitamin D in modulating both gut microbiota dysbiosis and immune system dysfunction, shedding light on the possible relevance of an adequate intake of this nutrient in the primary prevention of AITD and CeD. While future technology-based strategies for proper vitamin D supplementation could be attractive in the context of personalized medicine, several issues remain to be defined, including standardized assays for vitamin D determination, timely recommendations on vitamin D intake for immune system functioning, and longitudinal studies and randomized controlled trials to definitely establish a causal relationship between serum vitamin D levels and the onset of AITD and CeD.

Effectiveness of selenium supplementation in children with autoimmune thyroiditis

Deficiencies of Selenium (Se) is correlated with the risk and onset of autoimmune thyroid disease (AITD). The aim of this study was to determine the association between Se supplementation and AITD. Methods: Electronic data searches of 4 databases were performed. We assessed the included studies using PRISMA for protocol assurance. Five studies met our inclusion criteria and were analyzed. The predictor covariate in the present study was Se administration. The outcome measures were levels of thyroid peroxidase antibodies (TPO-Ab), thyroglobulin antibody (Tg-Ab), free thyroxine (fT4), and thyroid volume. Results: Of the five studies that met the inclusion criteria, one randomized controlled trial (RCT) was included in the qualitative review, whereas four quasi-experimental studies were included in the meta-analysis. The results showed that Se supplementation significantly reduced TPO-Ab levels (MD 90.85; 95% CI 61.71–120.00; p<0.00001) and fT4 levels (MD 1.52; 95% CI, 0.55–2.50; p=0.002), while the RCT showed that Se supplementation significantly reduced Tg-Ab levels. Conclusions: Se supplementation significantly reduces TPO-Ab and fT4 levels in children and adolescents with AITD. The limited number of studies and population sizes emergence of further studies especially RCTS are needed to make a better meta-analysis

Gender Differences at the Onset of Autoimmune Thyroid Diseases in Children and Adolescents.

Background: The incidence of autoimmune thyroid diseases (ATD) may vary with the beginning of reproductive function, although few reports differentiate the incidence before and during the onset of puberty, examining gender bias. We analyzed onset of ATD in a pediatric population to assess gender differences in onset age, disease subtype, pubertal status, autoimmune co-morbidity, family history and treatment, focusing on the interaction between gender and pubertal stage.Patients and methods: We retrospectively recorded 382 children and adolescents with ATD. In each patient physical examination was considered. The presence of other associated autoimmune diseases (AAD) and familial predisposition was also recorded.Results: Predominant prevalence was noted in females compared to males (p < 0.001), both in Hashimoto's diseases (HD or HT) and Graves' disease (GD) (p < 0.001). Mean age at diagnosis showed no significant difference between sexes (p > 0.05). A higher prevalence in pubertal subjects was noted compared to prepubertal (p < 0.001, particularly HT in early and GD in late pubertal stage), without sexes difference intra-(prepubertal vs. pubertal) and inter-puberty groups (prepubertal vs. early pubertal vs. late pubertal). Both in HT and in GD, the prevalence of autoimmune associated diseases (AAD) was higher in males compared to females (p = 0.04), with similar distribution according to the pubertal maturation. The familial predisposition was similarly distributed in both genders (p > 0.05) and into pubertal stages (p > 0.05).Conclusions: Females are more prone to develop ATD during puberty, earlier in HT than in GD. The effect of puberty is not different between genders, suggesting the role of additional factors other than hormones. The screening for detection of ATD is recommended in all patients with positive family history and other autoimmune diseases, mostly in males. Considerations of gender in pediatrics could be important to define pathogenic mechanisms of ATD and to help in early diagnosis and clinical management.

Effects of acute psychosocial stress on the hypothalamic-pituitary-thyroid (HPT) axis in healthy women

ObjectiveThe individual set point of the hypothalamic-pituitary-thyroid (HPT) axis is largely genetically determined. Apart from this genetic predisposition, the HPT axis may also be malleable to environmental demands such as psychosocial stress. Indeed, previous research has indicated that critical life events often precede the onset of autoimmune thyroid diseases, and subtle abnormalities in HPT functioning are present in some patients with stress-related disorders such as depression. However, no studies have investigated whether exposure to psychosocial stress leads to an immediate activation of the HPT axis. MethodsA total of N = 30 healthy women attended two laboratory appointments in a randomized order. An intravenous catheter was inserted at the beginning of each appointment. In the stress session, this was followed by the Trier Social Stress Test (TSST). Plasma samples to determine thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were taken at baseline and 20, 50, and 110 min after the TSST started. In the control session, participants rested and were instructed to read magazines, while the sampling schedule was maintained. ResultsThere was a significant rise in TSH concentrations in response to the TSST, with a peak observed 20 min after stressor onset, and a steady decline thereafter. No such response was observed in the control session. The TSST did not increase T3 or T4. ConclusionThe finding that acute psychosocial stress is able to elicit a significant increase in TSH is relevant to our understanding of a number of stress-related illnesses presenting with abnormalities of the HPT axis.

Bacterial virulence antigens and the pathogenesis of autoimmune thyroid diseases (AITD).

There is now substantial evidence that autoimmune thyroid diseases (AITD) coincide with a subclinical persisting infection with Yersinia enterocolitica (YE) which manifests through humoral and cellular immune reactions against YE at the onset of AITD. The humoral and cellular crossreactivities of YE with thyroid autoantigens are exclusively directed against conformational epitopes of YE membrane associated antigens and of YE plasmid encoded virulence proteins (YOPs). Especially, the outer membrane domain of the TSH-Receptor (THSR) appears to have conformational homologies with YE antigens. Immunological- and molecular findings, however, do not allow definite conclusions about a potential role of YE-infection in AITD, although the evidence is suggestive. Recent investigations on the effect of YE-superantigen (Sag) on T-cells from patients with AITD as well as AITD like manifestations in YE immunized mice and rats may yield more conclusive information about the role of YE infection in the pathogenesis of AITD.

Regulatory CD8 + T cells control thyrotropin receptor-specific CD4 + clones in healthy subjects

One of the mechanisms ensuring immunological unresponsiveness or tolerance depends on the action of CD8 + lymphocytes. In this paper, we report that, in healthy subjects, a subset of CD8 +CD28 − T cells suppresses the specific response to TSH receptor (TSHR) of CD4 + clones. Suppression was highly specific, required cell–cell interaction, and was not mediated by cytotoxicity. Co-incubation of CD8 + and CD4 + clones, followed by the removal of the CD8 + cells from the cultures before testing CD4 + responsiveness to TSHR, demonstrated that CD4 + cells were anergic since they showed low response to the antigen and a significant impairment of IL-2 production. In CD8-mediated anergy induction, the T-cell receptor (TCR) on both CD4 + and CD8 + cells seems to play a role. Our results indicate that one of the mechanisms ensuring peripheral tolerance involve CD8 +CD28 − cells. A disregulation in the control of autoreactive clones by this subset might be important for the onset of autoimmune thyroid diseases.